In GC cells with HGF/c-MET activation, excessive transphosphorylated c-MET molecules are likely to interact with other receptor tyrosine kinases such as EGFR and HER2 forming heterodimers, which may allow bypass signaling to provoke resistance to corresponding targeted therapies.260–262 This provided a clue that co-inhibition of bypassing pathways may be a potential therapeutic application in treating GC. Here, MET is linked to gastric cancer.